Supernatants from human glioblastoma cell lines suppressed in vitro- generated cellular immune responses. These supernatants contained IL-6 but not other cytokines. Short-term (minutes) incubation of these supernatants with monocytic or dendritic antigen-presenting cells (APC) of healthy individuals resulted in decreased IL-12 and increased IL-10 production. Other GCS-induced changes in these APC include reduced expression of MHC class II and CD80/86. Such GCS-modified monocytes induced anergy and apoptosis in T lymphocytes. GCS induces the production of IDO (indoleamine 2,3-deoxygenase) that catabolizes tryptophan, thereby disrupting the T cell cycle. Human GCS was also used to treat mice, resulting in delay of skin allograft rejection. Supernatants from some but not all melanoma and ovarian tumor cell lines induced similar changes. The GCS model raises the possibility that tumors may escape immune surveillance by aberrant antigen presentation to tumor specific T cells, resulting in their deletion by apoptotic T cell death. HPV-infected women were studied for T cell responses to HPV E6 and E7 peptides, as well as to other immune stimuli. Patients who were HPV-positive with no sign of disease responded to E6 and E7. Patients with cervical dysplasia exhibited reduced immune function in general, and were unresponsive to E6 and E7. The extent of immune dysfunction was related to the extent of cervical dysplasia. Homosexual men who were HPV-positive were also studied for Th function. E6 and E7 responses were observed in patients with anal dysplasia. Immune functional defects were limited to patients who were positive for HIV. These patients exhibited reduced responses in general and were unresponsive to the E6 and E7 peptides. - cancer, cervical dysplasia, HPV, immune dysfunction, cytokines, glioma, antigen- presenting cells, - Human Tissues, Fluids, Cells, etc.